Published data and reports indicate that the members of the ELRCXC subfamily of CXCL chemokines are elevated in a number of diseases. There are a total of 16 CXCL family members. The chemokines are reported to be up-regulated in a number of inflammatory diseases, including COPD, in which CXCL1-3, 5, and 8, also known as Gro-α, -β, -γ (Haskill, S., et al. Proc. Natl. Acad. Sci., 1990: 87, 7732-7736), ENA-78 (Wang, D. and Richmond, A., Cytokine Reference. Oppenheim, J. J. and Feldman, M. ed., Academic Press, London, 1023-1027, Powerm C. A. et al. Gene., 1994: 151, 333-334), and IL-8 (Iizasa, H. and Matsushima, K., Cytokine Reference. Oppenheim, J. J. and Feldman, M. ed., Academic Press, London, 1061-1067, Matsushima, K. et al., J. Exp. Med. 1988: 167, 1883-1893) respectively (Am. J. Respir. Crit Care Med., 163: 349-355, 2001, Am. J. Respir. Crit Care Med., 168: 968-975, 2003, Thorax, 57: 590-595, 2002). It has be postulated that prolonged and elevated expression of these chemokines could be involved in the development of diseases such as COPD, osteoarthritis, rheumatoid arthritis, erosive arthritis, asthma, atherosclerosis, inflammatory bowel disease, psoriasis, transplant rejection, gout, cancer, acute lung injury, acute lung disease, sepsis, ARDS, peripheral artery disease, systemic sclerosis, neonatal respiratory distress syndrome, exacerbation of asthma and COPD, cystic fibrosis, diffuse panbronchiolitis, reperfusion injury, or endometriosis. These CXC chemokines are known to stimulate neutrophil chemotaxis by engaging and activating the CXCR1 and/or CXCR2 receptors. Thus the inhibition of these chemokines could prevent inflammatory cells from infiltrating the lung tissue and thus prevent tissue damage. The present invention is directed to inhibiting the activation of CXCR1 and CXCR2 receptors by using an antibody having the ability to bind to human IL-8, Gro-alpha, Gro-beta, Gro-gamma, and ENA-78, i.e. a penta-specific antibody.